Errors in blood pressure measurement Nursing project essay
December 3, 2021
Quality improvement initiative: Nursing shortage essay
December 3, 2021


Pulmonary and Renal Systems

Pulmonary and Renal Systems 

Case 1 

Respiratory diseases alter the air pathways which can alter gas exchange and may also interfere with air passage in the pulmonary and respiratory system (Bourdin, Burgel, Chanez, Garcia, Perez, & Roche, 2016). The subject in the current case is a female who has been diagnosed with chronic bronchitis and emphysema. These conditions affect her physiological functions of the respiratory and pulmonary system in various ways, as discussed below.

Changes that Led to Obstructions and Increased Air Resistance

The patient mentioned above has a chronic obstructive pulmonary disease (COPD), which is causing a contraction in the airways (Bourdin et al., 2016). The condition also increases mucus production, which thickens the connective tissues surrounding the airways, thus increasing air resistance (Bourdin et al., 2016). Another physiological effect of COPD is the destruction of the alveoli tissues and capillaries (Bourdin et al., 2016). The damage causes abnormal large air spaces, thus reducing the surface area for gas exchange (Bourdin et al., 2016).

How an Increased PaCO2 in Respiratory Acidosis Alters the Delivery of Oxygen

Respiratory acidosis causes alveolar hypoventilation (Bourdin et al., 2016). Hypoventilation increases the arterial Carbon dioxide concentration, which prevents gas exchange (Bourdin et al., 2016). Reduced gas exchange in turn reduces the delivery of oxygen to the lungs (Bourdin et al., 2016). 

The V/Q Ratio 

The V/Q ratio is a ratio of the amount of air reaching the alveoli to the amount of blood reaching the alveoli per minute (Bourdin et al., 2016). The ratio helps to determine the blood oxygen and carbon dioxide concentration. The V/Q in the patient, in this case, has been reduced  by chronic bronchitis and emphysema (Bourdin et al., 2016). 

Why the Patient has Ankle Edema 

Chronic obstructive pulmonary disease may cause heart failure, which makes the forward  motion of blood moving from the lungs to the heart difficult (Bourdin et al., 2016). The failure of  the heart causes an increased hydrostatic pressure in the pulmonary vasculature (Bourdin et al.,  2016). The elevated hydrostatic pressure leads to an imbalance in the Starling’s forces in the  pulmonary capillaries (Bourdin et al., 2016). This increases interstitial fluid accumulation  leading to pulmonary edema (Bourdin et al., 2016).  Oxygen diffusion from the alveolus increases the pressure of the pulmonary artery  (Bourdin et al., 2016). An increase in pressure on the pulmonary artery may, in turn, cause a  strain in the right ventricle of the heart which can lead to heart muscle weakness or failure  (Bourdin et al., 2016). 

Case 2 

Renal System 

A block in one renal artery triggers the release of renin to increase renal blood flow  (Derkx & Schalekamp, 2014). On the other hand, if the other renal artery is not blocked, there  will be a drop in renin production to reduce renal blood flow on that artery thus reduce blood  pressure (Derkx & Schalekamp, 2014). A low renin production in the normal renal artery is an  attempt to maintain balanced blood pressure (Derkx & Schalekamp, 2014). 

Function of Renin 

Renin plays a role in controlling blood pressure. First, it stimulates a protein known as  angiotensinogen to release angiotensin I (Derkx & Schalekamp, 2014). Angiotensin I further  metabolized to form angiotensin II (Derkx & Schalekamp, 2014). Angiotensin II causes the  constriction of arterioles, thus creating a rise in blood pressure (Derkx & Schalekamp, 2014).  Renin also increases blood flow to the arteries, thus increasing blood pressure (Derkx &  Schalekamp, 2014). It also increases the amount of sodium in the distal tubule, which also leads to a rise in blood pressure (Derkx & Schalekamp, 2014). Renin also stimulates the sympathetic  nervous system, which also causes a blood pressure rise (Derkx & Schalekamp, 2014). 


The medications that can prevent adverse high blood pressure effects include diuretics  and angiotensin-converting enzyme (ACE) inhibitors (Safian & Textor, 2017). ACE inhibitors  are appropriate because they block the formation of angiotensin II, thus preventing high blood  pressure (Safian & Textor, 2017). Diuretics, on the other hand, help to prevent high blood  pressure since they eliminate excess sodium from the body, thus preventing a rise in blood  pressure (Safian & Textor, 2017).


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